Neurodegenerative disorders leading to dementia, such as Alzheimer?s disease (AD) are chronic, long term processes resulting from an accumulation of various lesions and insults to the brain. Investigators at The National Institute of Neurological Disorders and Stroke (NINDS) of the National Institute of Health (NIH) reported a therapeutic approach to neurodegenerative disorders such as AD using a truncated peptide derived from the cyclin-dependent kinase 5 (Cdk5) activator P35, which specifically inhibits the deregulation activity of Cdk5, thereby rescuing the cortical neuronal phenotypes responsible for neuronal damage in AD model mice. A transgenic mouse model (5XFAD) was used for this study since the brains of these mice display the hallmark AD tau and A? pathology accompanied by significant behavioral defects. Age-matched wild-type (WT) mice were identified by genotyping and used as a control group. These results were published by Shukla, V et al: A truncated peptide from p35, a Cdk5 activator, prevents Alzheimer?s disease phenotypes in model mice. FASEB J. 27, 174 186 (2013).